Giuseppe
Emeritus
[Source: Eurosurveillance, full text: (LINK). Abstract, edited.]
F Gobbi (
)<SUP>1</SUP>, Z Bisoffi<SUP>1</SUP>
Citation style for this article: Gobbi F, Bisoffi Z. Human African trypanosomiasis in travellers to Kenya. Euro Surveill. 2012;17(10)
ii=20109. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20109
Date of submission: 07 March 2012 <HR>
In this issue, two cases are described of human African trypanosomiasis (HAT) due to Trypanosoma brucei rhodesiense. They occurred recently in European tourists returning from Masai Mara area, Kenya, to Germany and Belgium, respectively [1,2]. These are, to our knowledge, the first two HAT cases described in travellers to Kenya in the last 12 years, while several cases were reported mainly from Tanzania (Serengeti and Tarangire game parks), Zambia, Zimbabwe and Malawi [3]. HAT, also known as sleeping sickness, is caused by a flagellated trypanosome protozoan, which is transmitted by Glossina (tsetse) flies. T. b. gambiense ? found in western and central Africa ? is transmitted mainly by G. palpalis, which prefers areas of vegetation near rivers and cultivated fields; T. b. rhodesiense ? found in eastern and southern Africa ? is transmitted predominantly by G. morsitans, which feeds on wild animals in savannah areas, far from human settlements [4]. While humans are the only substantial reservoir of T. b. gambiense, T. b. rhodesiense HAT is a zoonosis and humans occasionally visiting affected areas (usually for hunting or tourism) are accidental hosts. T. b. gambiense HAT is usually characterised by a chronic course of illness, lasting months to years, whereas T. b. rhodesiense HAT causes a more acute and aggressive course, clinically resembling acute septicaemia or severe falciparum malaria, with death occurring within days, weeks or months of the untreated disease. HAT of both forms is characterised by two distinct phases: the early or haemo-lymphatic stage and the late or meningo-encephalitic stage, with trypanosome invasion of the central nervous system of patients surviving the early stage [5]. (?)
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Eurosurveillance, Volume 17, Issue 10, 08 March 2012
Editorials
Human African trypanosomiasis in travellers to Kenya
Editorials
Human African trypanosomiasis in travellers to Kenya
F Gobbi (
- Centro per le Malattie tropicali, Ospedale Sacro Cuore-Don Calabria, Negrar, Verona, Italy
Citation style for this article: Gobbi F, Bisoffi Z. Human African trypanosomiasis in travellers to Kenya. Euro Surveill. 2012;17(10)
Date of submission: 07 March 2012 <HR>
In this issue, two cases are described of human African trypanosomiasis (HAT) due to Trypanosoma brucei rhodesiense. They occurred recently in European tourists returning from Masai Mara area, Kenya, to Germany and Belgium, respectively [1,2]. These are, to our knowledge, the first two HAT cases described in travellers to Kenya in the last 12 years, while several cases were reported mainly from Tanzania (Serengeti and Tarangire game parks), Zambia, Zimbabwe and Malawi [3]. HAT, also known as sleeping sickness, is caused by a flagellated trypanosome protozoan, which is transmitted by Glossina (tsetse) flies. T. b. gambiense ? found in western and central Africa ? is transmitted mainly by G. palpalis, which prefers areas of vegetation near rivers and cultivated fields; T. b. rhodesiense ? found in eastern and southern Africa ? is transmitted predominantly by G. morsitans, which feeds on wild animals in savannah areas, far from human settlements [4]. While humans are the only substantial reservoir of T. b. gambiense, T. b. rhodesiense HAT is a zoonosis and humans occasionally visiting affected areas (usually for hunting or tourism) are accidental hosts. T. b. gambiense HAT is usually characterised by a chronic course of illness, lasting months to years, whereas T. b. rhodesiense HAT causes a more acute and aggressive course, clinically resembling acute septicaemia or severe falciparum malaria, with death occurring within days, weeks or months of the untreated disease. HAT of both forms is characterised by two distinct phases: the early or haemo-lymphatic stage and the late or meningo-encephalitic stage, with trypanosome invasion of the central nervous system of patients surviving the early stage [5]. (?)